Autophagy constitutes a catabolic process involving lysosomal degradation of damaged and redundant cytosolic components into biomolecules, via an elaborate lysosomal pathway. Autophagy is a highly regulated and evolutionary conserved process crucial for normal tissue homeostasis and cell life. Certain members of the Bcl-2 gene family, including the BH3 only protein Bnip3 regulate autophagy during cardiac stress during ischemic or hypoxic injury as means of discarding damaged mitochondria and organelles to avert cell death. Defects in the regulation of autophagy have been associated with a number of human pathologies including cancer, neurodegenerative diseases, and heart failure. Here, we discuss the molecular regulation of autophagy in the heart and cellular demise from “too much a good thing.”
*Departments of Physiology
†Pharmacology and Therapeutics, The Institute of Cardiovascular Sciences, St Boniface Hospital Research Center, Faculty of Medicine, University of Manitoba, Winnipeg, MB.
Reprints: Lorrie A. Kirshenbaum, PhD, Departments of Physiology and Pharmacology and Therapeutics, Institute of Cardiovascular Sciences, St Boniface General Hospital Research Center, Room 3016, 351 Taché Avenue, Winnipeg, Manitoba, Canada R2H 2A6 (e-mail: email@example.com).
Supported by grants to L.A. Kirshenbaum is a Canada Research Chair in Molecular Cardiology from the Canadian Institutes of Health Research (CIHR) and Heart and Stroke Foundation of Canada (HSFC); J.W. Gordon is supported by a CIHR-MHRC Fellowship and the IMPACT Strategic Training Program.
The authors declare no conflicts of interest.
Received December 8, 2011
Accepted January 24, 2012